Fibrinogen Deposition on Silicone Oil-Infused Silver-Releasing Urinary Catheters Compromises Antibiofilm and Anti-Encrustation Properties

Slippery silicone-oil-infused (SOI) surfaces have recently emerged as a promising alternative to conventional anti-infection coatings for urinary catheters to combat biofilm and encrustation formation. Benefiting from the ultralow low hysteresis and slippery behavior, the liquid-like SOI coatings have been found to effectively reduce bacterial adhesion under both static and flow conditions. However, in real clinical settings, the use of catheters may also trigger local inflammation, leading to release of host-secreted proteins, such as fibrinogen (Fgn) that deposits on the catheter surfaces, creating a niche that can be exploited by uropathogens to cause infections. In this work, we report on the fabrication of a silicone oil-infused silver-releasing catheter which exhibited superior durability and robust antibacterial activity in aqueous conditions, reducing biofilm formation of two key uropathogens Escherichia coli and Proteus mirabilis by ∼99%, when compared with commercial all-silicone catheters after 7 days while remaining noncytotoxic toward L929 mouse fibroblasts. After exposure to Fgn, the oil-infused surfaces induced conformational changes in the protein which accelerated adsorption onto the surfaces. The deposited Fgn blocked the interaction of silver with the bacteria and served as a scaffold, which promoted bacterial colonization, resulting in a compromised antibiofilm activity. Fgn binding also facilitated the migration of Proteus mirabilis over the catheter surfaces and accelerated the deposition and spread of crystalline biofilm. Our findings suggest that the use of silicone oil-infused silver-releasing urinary catheters may not be a feasible strategy to combat infections and associated complications arising from severe inflammation.


S2
1. As the oil diffuses into the silicone catheter, measuring the weight of the swelling oil cannot be used to find the thickness of the surface oil layer. By assuming that the silicone catheters swell isotropically, however, measurements of weight and volume before swelling, after swelling, and after wiping could be used to approximate the layer thickness and volume of infused oil. By solving a cubic polynomial function, the oil thickness can be calculated.
In brief, the weight (m 1 ) of the original catheter was measured. The weight (m 2 ) and the dimensions (x,y,z) of the swollen catheter after wiping were also measured. A total of 6 replicates were used for the measurements. Due to the nature of physical absorption, the oil thickness (t) is assumed uniform in all directions. The oil thickness is then determined using the following equation: 1 -2 where x, y, z are the length, width, and height of the swollen catheter, respectively. The oil density (ρ) used in this study was 0.93g/cm 3 . In this study, the measured oil thickness was estimated to be 30.3 ± 6.1 μm.

2.
To investigate the effect of oil thickness on bacterial adhesion, we further prepared AgO samples with a coating thickness of ~ 14 μm (AgO-1). The coating thickness was calculated using equation a.
The release of Ag + in neat PBS and Fgn-supplemented PBS was determined by ICP-OES, Fgn adhesion was assessed by the BCA method, and effect of Fgn adsorption on antibiofilm activity was determined by a plate count method after 24 h and compared with AgR and AgO (thickness of ~ 30 μm). Figure S1a, the thinner oil layer in the AgO-1 resulted in a slower release of Ag + in PBS when compared with the AgO. According to equation a, the reduced oil adsorption in AgO-1 led to a lower swelling ratio in all directions when compared with the AgO, and this may hinder the leaching of loosely bonded AgNPs upon water flushing. In the presence of Fgn, the release of Ag + from all the samples was retarded, indicating that absorbed protein hindered silver release and this may further block the interaction of antibacterial Ag + with bacteria. Further, we assessed the effect of oil thickness on Fgn adhesion. As shown in Figure S1b, no significant difference (p>0.05) in Fgn adhesion was observed between the AgO and AgO-1 samples. This indicated that the silicone oil layer was stable during the S3 test and could facilitate Fgn adsorption regardless of oil thickness. To investigate the effect of oil thickness on biofilm adhesion, the number of viable cells attached to different surfaces was counted and compared. For both strains, no significant difference (p>0.05) was noted in the number of attached viable cells on the AgR, AgO and AgO-1 surfaces. This result is consistent with the ICP results in Figure S1a. Overall, the silicone oil layer facilitated Fgn adsorption on the AgO and AgO-1 surfaces regardless of oil thickness and the deposited Fgn blocked the interaction of silver with the bacteria, resulting in a compromised antibiofilm activity. Figure S1. (a) silver release profiles from AgR, AgO, and AgO-1 in PBS and Fgn suspension over time;

As seen in
(b) Fgn adsorption on Ag, AgO, and AgO-1 surfaces after 24 h; (c) Quantitative counts of viable E. coli and P. mirabilis cells adhering to Ag, AgO, and AgO-1 surfaces after 24 h of incubation (n = 6, bars represent standard deviation of the mean).